Respiration Flashcards
Define tidal volume, respiratory rate and pulmonary ventilation rate
Tidal volume = normal volume expired on a breath (not forced)
Respiratory rate = breaths per minute
Pulmonary ventilation rate = air in and out in one minute = tidal volume x rr
States boyles law, Charles law and the universal gas law
Boyles law = pressure is inversely proportional to volume.
Charles law = pressure is directly proportional to temperature
Universal gas law= pressure x vol = temperature x gas constant
What is a meatus?
Channel formed by nasal conchae (turbinates) superior middle and inferior.
Define partial pressure, vapour pressure, tension and saturation vapour pressure.
Partial pressure - pressure (number of collisions of gas against a container) of just one gas in a mixture.
Vapour pressure - partial pressure of water above a surface of water
Tension - a gases’ tendency to escape a liquid
Saturation vapour pressure - the maximum pressure of water vapour in equilibrium with the liquid phase. Depends on temperature.
What is an olfactory region?
Region without as much mucous secretions for smell. Thick epithelia. Washed by serous secretions. Non olfactory have venous sinuses in LP that swell so that air only goes through 1/2 of nose
Describe 4 para nasal sinuses and their use
Sphenoidal
Ethmoidal
Maxillary
Frontal
Composition of glottis
Plicae vocales (true) attached to the arytenoid cartilage (posterior to larynx and thyroid cartilage and superior to cricoid cartilage) Vestibular folds (false) In between in the rima glottidis
Cartilage in lower respiratory tract?
Trachea C shaped and fibroelastic membrane with trachealis.
Primary bronchi - ring
Secondary and tertiary have a crescent, plates or islands
Bronchioles - none
Upper and lower and resp portion?
Sternal angle/ glottis
Bronchioles to alveoli.
Describe differences in ribs
1atypical - only have inferior facet on head, shortest, broadest, most curved.
2 atypical - no prominent costal groove
3-8- typical
9-10 typical but fuse to costal cartilage which joins costal cartilage of rib above not the sternum.
11-12 atypical ribs don’t fuse to cartilage, lie in diaphragm, only superior facet present on head, no tubercle
Describe the structure of a rib and it’s articulations
Head, superior and inferior facets (articulate with Demi facets of vertebral bodies) separated with crest
Neck - tubercule inferior laterally which articulates with transverse facet of vertebrae. (Costotransverse joint)
Costal groove found inferior, arteriorly
What is the costal margin?
Where costal cartilages form a V towards the sternum
Describe the intercostal muscles function and innervation.
External (anterior and inferior), hands in pockets, raises ribs, inspiration
Internal (anteriorly) and innermost(laterally), 90 deg, depresses ribs, forced expiration.
Supplied by anterior rami of corresponding nerve
Describe the structure of the diaphragm
Muscle ribs start from ribs, arcuate ligaments (median, lateral and medial) ad right and left Cruz and go to the central tendon.
Describe the distribution of intercostal nerves arteries and veins and their roots and what the nerves supply. Including supply and drainage
Artery- anastomoses between aorta and internal thoracic artery.
Vein - drains into azygous vein (SVC) (some into internal thoracic vein)
Nerve - anterior rami, supplies muscles, skin and costal and cervical parietal pleura.
Found in costal groove and just superior to rib
Phrenic nerve innervation.
3,4,5
Diaphragm, sensory to mediastinal and diaphragmatic pleural and the pericardium. Both surfaces of diaphragm.
Describe the pleural cavity and the lines of pleural reflection
Costal, cervical, diaphragmatic and mediastinal
Describe the mediastinal and their contents
Superior mediastinum. Bounded superiorly by thoracic inlet, inferiorly by T4- angle of Louis/ pericardium. Contains oesophagus, tachea, muscles, phrenic nerve, deep and superior cardiac plexuses, arch of the aorta, thymus, SVC, vagus, muscles
Anterior mediastinum - chest wall and fibrous pericardium. Thymus in kiddies, long thoracic vein and artery, sternophrenic ligament
Posterior mediastinum - descending/thoracic aorta, azygous vein, oesophagus, thoracic duct, vagus nerve, splanchnic nerve, sympathetic veins and trunk
Locations of PV, PA and bronchus in right and left hilum
Bronchi anterior Veins posterior 3/2 Left artery superior Right arteries (2) middle Lymph nodes between veins
What is the rate of diffusion in the lungs usually limited by?
Not area, or pressure, diffusion barrier - 5 layers
Describe the properties of the mechanical system comprising the lungs, chest wall and diaphragm
Lungs: elastic tissues for recoil
Chest wall: draws chest out via pluera to increase AP
Diameter: contracts to draw chest down increasing sup/infer
Muscles in forced inhalation and expiration?
Inspiration: external costal, diaphragm, serratus anterior, pec minor, scalene, sternocleidomastoid
Expiration: innermost and internal intercostal muscles, abdominal muscles
Define functional residual capacity, residual volume, vital capacity and inspiratory capacity
Tidal vol - total volume breathed in and out on a normal breath/ displaced with no extra effort.
Inspiratory reserve vol- extra volume than can be inspired than normal
Exploratory reserve vol - extra vol that can be expired than normal
Inspiratory capacity - total amount that can be inhaled after a normal exhale.
Residual vol - air left in lungs after a forced expiration
Functional residual capacity- air left in lungs after a normal expiration
Vital capacity- maximal amount that can be inhaled from the RC
Serial dead space, physiological dead space and how these variables are measured
Serial dead space= non collapsible structures- bronchi upwards. Air in structures that do not take part in gas exchange - 150ml. (Conducting airway)
Measured via nitrogen washout, forced expiration, forced inspiration of 100% O2, amount of N2 measured and use to calculate volume.
Physiological dead space= serial dead space + alveolar dead space (gas in alveoli that can’t take place in gas exchange).
Looking at pO2 and pCO2 breathed out compared with normal alveolar pressures as alveolar air is dilated by dead space air.
What is alveolar ventilation rate and how is it calculated?
Tidal volume - physiological dead space * respiratory rate
Define compliance of the lungs and how it is measured
Stretchiness of lung, higher means more stretch.
Change in vol/ change in pressure
Factors which affect compliance
Surface area. As surface area increases then compliance decreases. This is due to water tension.
Surfactants decrease water tension so increase compliance
What is hysteresis?
No all energy put into stretching lungs on inspiration is released on recoil. Greatest when tidal vol is maximal.
Why do big bubbles eat little bubbles? (Or not)
Laplaces law = 2x SA/ radius = pressure
High bubbles have a lower pressure so eat small bubbles.
Surfactant decreases water tension so bub les are stabalised- less in big bubbles so a higher tension.
Factors which affect airway resistance and how resistance changes over a breathing cycle.
Poiseulles law. Resistance through a tube is inversely proportional to radius. Larger radius then lower resistance. Tubes narrow on expiration so more resistance. Compliance also affects how much we can inhale.
Describe spirometry
Measures FVC. Can link to a vitalograph to measure over time.
Limited by compliance, for e of muscles and airway resistance
Describe FVC and FEV1.0
Force vital capacity and forced expiratory vol in one second
On vitalograph
Explain obstructive and restrictive patterns of spirometry.
Obstructive then lower fev e.g. Asthma
Resistrictive the lower FVC e.g. Fibrosis and chest wall probs
Explain inspiratory and expiratory flow volume loops and how they are affected by upper and lower airway obstructions
Peak flow meter
PEFR
Decrease in flow after peak flow (at higher vols) unless severe.
Describe the measurement of residual volume
Helium dilation - not taken into blood stream. Measure difference in conc.
Describe the measurement of transfer factor.
CO, only limited by diffusion barrier. Binds to haem readily. Measure differnces in conc for TF
State the solubility of O2 in body fluid
0.01mmol/l/kPA at 37
What are the normal values of alveolar and capillary pO2?
13.3
5kPa
Properties of haemoglobin that makes it good
Tetromer. Exists in two states. Tense hard to bind Relaxed easy to bind More PO2 then more R Highly reversible. Lower O2 at tissues so more delievered. High temp and H+ cause more T
Effects on the dissociate curve of a high temp/ fall in pH
Right left, harder to bind
Estimate rate of delivery of O2 to tissues at different capillary pO2s and pHs
Haem found at 2.2 mmol/ l and bind 4 O2.
Use graph and O2 saturation at different pressures
Factors affecting gas diffusion in alveoli
Thickness of barrier/ resistance to diffusion
Partial Pressure gradient
Area
How is the transfer factor obtained/ diffusion capacity
Vital capacity containing CO. Exhale, how much CO is there now? pCO in blood =0 and so all that can transfer will have. First 750ml is discarded. Helium used to measure dilution effects.
Reactions of CO2 in blood
CO2+H20 = HCO3 + H
In mito, more HCO3 produced so equilibrium to left.
Dissolved CO2 affects pH
What is the Henderson hasselbach equation a and calculate pH given pCO2 and HCO3
PH= pK (6.1) + log( HCO3/(CO2*0.23))
Factors affecting HCO3 conc
H+ reacts with haemoglobin so more HCO3 produced and leaves RBC via AE
Kidney maintain long term via reabsoption
Buffering action of haem in RBC
High CO2 then H+ binds to HCO3 and haem
Low CO2 then Co2 reacts with H2O to form more H+/ dissociates from haem
Function of carb amino proteins
Binds to CO2 so that it cannot dissolve. This co2 therefore has no effect on pH. Transport molecules
Normal content of CO2 in arterial and venous blood
21.5mmol/l in arterial
23.5 mmol/l in venous
Haem can bind more H+ without O2 in venous so blood can carry more CO2 without pH changing
State the proportion of CO2 travelling in various forms.
80% HCO3
11% carbamino
8% dissolves CO2
Define hypoxia hypocapnia, hyperventilation and hypoventilation
PCO2<8
Low CO2 (3.5?)
RR 12-20
Effects on plasma pH of hypo and hyper ventilation and the result
Effects co2, effects pH.
Acidosis- coma, seizures, arrhythmias, vomiting, nausea
Alkalosis- fainting, dizziness, coma, free Ca decrease so tetany
Define respiratory acidosis and alkalosis, compensated respiratory acidosis and alkalosis
Due to over/ under ventilation/perfusion rise/fall in CO2 so pH effects.
Compensated by kidney- removal of HCO3 or retention
Define metab acid/alk and compensated?
Due to metabolic cause e.g. Ketoacidosisis or lactic acidosis or antifreeze or vomiting.
Compensated quickly by ventilation
Describe acute effects upon ventilation of falling pO2, increase in inspired pCO2 and falls in arterial plasma pH.
All increase
Location and function of central chemoreceptors. Roles if the cerebrospinal fluid (CSF) blood brain barrier and choroid plexus in the response
Medulla around CSF. Detect pH only affected by CO2 which freely diffuses but HCO3 does not. If increaesed/ decreased ventilation does not solve then HCO3 diffuse via choroid plexus to neutralise and stop.
Metabolic acidosis detection?
Peripheral as only change I’m HCO3??
Describe type 1 resp failure
Low O2 but normal or decreased CO2.
Occurs when problems in ventilation/perfusion or diffusion barrier. E.g. Pneumonia, PE
Breathlessness, central cyanosis, exercise intolerance
Describe type 2 resp failure
Low O2 me high Co2.
Problems with ventilation e.g. Chest wall probs, COPD, asthma, opioids
Acutely then breathlessness but compensation occurs and CSF equilibriates so driven by hypoxia. Can cause pulmonary hypertension due to contraction in response to hypoxia
How can arterial blood gases be measured?
Pulse oximetry
Describe ventilation/perfusion mismatch and diffusion impairment and how they can lead to type1. Outline the causes of each
Want to be 1 (0.8 is normal).
PE/ thicker barrier (pneumonia) means less perfusion so not all O2 breathed off
Describe how hypoventilation results in type 2 and outline its important causes
Fibrotic lung disease, COPD, emphysema (severe), severe asthma, scoliosis/ kyphosis
Define asthma and describe the nature of airflow obstruction in asthma
Chronic disease characterised by airway remodelling - thickening of SM and BM. Reversible airflow obstruction. Hypersensitivity/ increased airway responsiveness to a variety of stimuli.
Damaged epithelium due to chronic inflammation
More likely in females. Can be allergic (eosinophils, IgE and mast cells), asprin sensitive or occupational (farmers, welders and bakers)
Describe the pathophysiology of asthma
Mucins and hypersensitivity/ contraction and narrowing of airway make a reversible airflow obstruction.
To maintain flow pressure must change (r4) (poiseuilles equation)
Describe the precipitating factors for asthma attack
ACh release- muscurinic agonist, prostaglandins, leukotrienes, histamine, cold air
Allergens - dust mites, air pollution, fungal spores, HDM, pollens
Describe the signs and symptoms of asthma and their physiological basis
Dry cough- no infection- worse on exercise Respiratory wheeze Dispnoea Chest tightness Recession and tracheal tug Prolonged expiratory phase
Describe the tests used to assess the condition of a patient suspected of asthma and how they are interpreted
History- eczema, family history, prenatal smoking, occupation
Examination- hyperesonant, barrel chest,
Investigation- flow volume loop- restrictive, auscultation polyphonic wheeze.
lower FEV/FVC or normal, lower PEFR- 12% increase in FEV with salbutamol. bronchial hyper responsiveness- bronchial challenge test e.g, histamine.
FENO- released from inflammation.
Allergy testing
Sputum induction
Exercise induced bronchoconstriction- pre and post spirometry.
Principles of treating asthma
Prevent- smoking, allergens, exercise, housing, cleaning
B2 agonists
Muscurinic antagonists -ipratropium (anticholinergic)
Theophylline/ aminophylline (anti inflam)
Corticosteroids and leukotrienes receptor antagonist .
Acutely- IV drugs, interbate, ventilate, salbutamol and atrovent nebs, O2
Peripheral chemoreceptors location
Carotid and aortic bodies
Describe the major precipitating factors for asthmatic attacks
Lack of treatment adherence
Respiratory virus infections associated with the common cold
Exposure to allergen or triggering drug e.g. NSAIDS
Describe the main causes of COPD and the nature of airflow obstruction in COPD
Chronic bronchitis - inhaled irritants e.g. Smoking, cause chronic inflammation which damages muco-ciliary escillator, damages epithelium, increases mucous secretion with the result being narrowed airways
Emphysema - loss of elastin leading to destruction of alveolar walls, irritants and inflammation
Both are progressive and not fully reversible
Describe the signs and symptoms of COPD
Tachypnoea
Cough dry or productive worse at night
Infection
Barrel chest, hyper resonant due to hyperinflation and air trapping
Leaning forward- accessory muscles
Reduced intensity breath sounds
Reduced air entry, loss of elasticity and tissue breakdown increasing resistance and residual capacity.
Possible wheeze
May develop pulmonary hypertension, central cyanosis, Hypercapnia (flapping tremors.
MRC Dyspnoea scale
Investigations of COPD patients
Cxr- hyper expansion - flat diaphragm, more than 6 ribs, increased anteroposterior diameter, hyperlucent lungs, signs of pneumonia/ pneumothorax, rule out other stuff.
Pulse oximetry and ABG
Lung function tests- ratio under 70% and limited reversibility. Reduced FEV
Management of COPD patients
ACh blockers Ipratropium, bronchodilators- salbutamol.
Stop smoking
Exercise
Education
Surgery- remove bullae from emphysema, lung transplant,
Pneumonia vaccine
Oxygen therapy- prevent hypertension and relieve symptoms (not if breathless) long as possible, portable or just intermittent
Corticosteroid- decrease inflammation
Ventilate
Pulmonary rehab- increase exercise capacity
Outline normal flora of the GI tract
Viridens streptococci (a haemolytic), anaerobes, neisseria spp, Candida albicans
Sometimes:
Strep pneumoneai, pyrogens, h influenzae,
Rare:
E. coli, pseudomonas
Natural defenses of respiratory tract against infection
Muco ciliary escalator
Lymphatics, alveolar macrophages, IgA and IgG secreted
Cough and sneeze
Main infectious diseases of upper respiratory tract and the organisms commonly causing these infections
Sinusitis Parotitis Tracheitis Laryngitis Pharyngitis Otitis media Rhinitis - cold Epiglottitis
RSV
Coronovirus
Influenza
Rhinovirus
May lead to bacterial infection Meningitis Mastoiditis Brain abcess Common with sinusitis or Otitis media
Define the term pneumonia and distinguish between acute and chronic
Pneumonia- infection of lung parenchyma with consolidation (not compressible) and exudate
Acute/ lobar- one lobe affected normally CA and strep pneumoniae. May lead to emphyma, lung abscess or bronchiectasis (widened)
Chronic - bronchial- multiple lobes affected, widespread/ patchy consolidation, starts in bronchi, often hospital aquired, may cause heart failure, viral infections.
Describe the infectious aetiology of acute community acquired and acute hospital aquired pneumonias
Ca:
Common- strep pneumoniae, Haemophilus influenza, klebsiella pneumoniae
Atypical- chlamydia pneumophila, mycobacterium pneumoniae, legionella pneumophila
Viral- influenza, RSV
Ha- staph aureus, E. coli, pseudomonas aeriginosa,
Immunosupression- pneumocystis jirovecii, candida, aspergillus, viruses
List the aetiological clues for the common respiratory tract pathogen
Strep pneumoniae- elderly, co morbid Aspiration - E. coli Legionella- travelling H influenzae - COPD Mycoplasma- young, prior antibiotics, extra pulmonary involvement S aureus- drug user, post viral
Clinical features of pneumonia
Malaise Fever Cough- productive, can vary in sputum Dyspnoea Chest pain on inspiration Chills, sweats rigors Vomiting Anorexia Myalgia Diarrhoea Wheeze
Dull on percussion
Ausculation- crackles, wheeze, bronchial breath sounds
Investigations of pneumonia
CXR
Culture/ labs see other card
How do you assess the severity of pneumonia/ management?
Confusion urea >7 Resp rate over 30 Blood pressure less than 90 or 60 65 + 2+ = hospital 3+ = ICU
Understand the principles of collection of specimens for lab diagnosis of pneumoniae
Nose/ throat swab Sputum sample- bronchial/alveolar lavage Biopsy? Blood Urine- legionella Serotyping
Microscopy
Macroscopic - sputum
Culture- stain acid and alcohol fast
Antibody/ antigen detection
Common opportunistic pneumonia infections
Pneumocystis spp.
Aspiration e.g. Coma, alcoholics, epilepsy, dysphagia - E. coli and pseudomonas
Whooping cough- bordetella pertussis- culture and PCR, cough and vomit, erythromycin
Aspergillus and candida
Cytomegalovirus
Cryptosporidium Protozoa
Mycobacterium spp.
CF- haemophilus, s aureus, later pseudomonas auringinosa.
Describe the principles of anti microbial therapy in pneumonia and understand the rationale for selecting different antibiotics
Pneumococcus- amoxicillin or if severe then co-amoxiclav
If atypical then erythromycin,clarithromycin, doxycycline, levofloxacin for legionella.
Describe the microbiology of mycobacterium tuberculosis
Acid and alcohol fast bacilli.
Spread via aerosol
Describe the pathology of m tuberculosis
Acute- forms primary complex- sub pleural lesions Ghon’s focus and infects hilar lymph nodes. When they occur together they are called the primary complex. Can calico fly or spread.
Post primary infection - beyond first week, throughout body/ lung military spread. Cavitation of lungs and cytokines mediated systemic effects.
Spread to kidneys, limbo sacral spine, large joints, meningitis.
Describe the host response to a TB infection
Ingested by macrophage but prevents fusion of phagosome with lysosomes.
Escapes and multiplies in cytoplasm.
Provokes immune response - il2 then IFn-g and TNF a. Activate and recruit more macrophages causing granulomas
Describe the typical presentation and radiographic changes in resp TB
Dyspnoea Cough- wet or dry Haemoptysis Fever Primary - asymptomatic Tiredness and malaise Weight loss and anorexia.
Non specific signs, palor, fever, weigtloss, clubbing, lymph nodes
X ray changes - shadowing, cavities, consolidation, military seeds, Cardiomegaly, calcification.
Describe the primary and post primary changes in TB
Primary - swollen lymph possible
Post primary - symptoms especially cough, fevers and weight loss.
Describe lymph TB
Affects neck- internal thoracic, swollen, inflamed, may compress trachea/ bronchi
Describe orthopaedic TB
Spondylitis- sub chondral ossification along lateral ligaments - paraplegia and quadriplegia possible
Poncets disease- poly arthritis
Describe meningitis from TB
Headache, fever, confusion coma.
Normally from military TB
Describe pleural TB
Hypersensitivity response in primary infection
Or
Tuberculous Empyema with ruptured cavity through chest wall.
Describe miliary TB
Bacilli in blood from primary or reactivation.
Spread to multiple organs/ sites within lungs.
Diagnosis of TB
Clinical features
CXR
Sputum sampling- swab/ lavage, blood culture, biopsy
Describe the mechanisms of drug resistance in TB
Spontaneous mutations.
Poor adherence means multi drug resistant TB (mdrtb) increasing.
Describe the management of TB and side effects
Rifamipicin- hepatitis, rash, flu like symptoms, ARF, thrombocytopenic purpura
Isoniazid- hepatitis, rash, peripheral neuropathy
Pyrazinamide - hepatitis, rash, arthralgia
Ethambutol- optic neuritis
4 then 2 2 months and 6 months
Only infectious for 2 weeks
Poor adherence
Describe the BCG
Uses live attenuated bovine tuberculosis bacillus. Lasts 15 years. Variable efficacy.
Used for high risk groups
High risk groups TB
HIV Corticosteroids or anti TNF antibody Immunosuppressant Post surgery Silicosis Malnutrition IV drug Overcrowding Smokers and chronic lung disease Asians Diabetes
Describe the relationship between TB and HIV
Leading cause of death in HIV patients.
Much higher risk
Describe public health issues surrounding a case of TB
Immediate contact with TB radiology if suspected and treatment started immediately
Describe the incidence of lung cancer in different groups
Men 100 in 100000 mortality vs 40 in women
Linked to socioeconomic factors
Increasing in women and decreasing in men
Give an account of the aetiological factors involved in lung cancer
Smoking - most Radon Genetics Asbestos Diet
Describe the typical pattern of symptoms reported by patients with lung cancer
Primary- Haemoptysis, Dyspnoea, cough, chest pain, wheezing, post obstructive pneumonia
Regional mets- hoarseness, Dyspnoea - phrenic nerve, SVC obstruction, dysphagia
Distant mets - bone pain fractures, CNS features, vision, headache, confusion ect.
.
Where can lung cancer spread?
Brain, lymph, pericardium, lung, pleura. Liver, adrenals, bone
Describe common paraneoplastic syndromes associated with lung cancer and understand the structural abnormalities underlying them
Paraneoplastic- endocrine cushings,SIADH, hypercalcaemia
Neurological - encephalopathy, peripheral neuropathy, eaton-lambert syndrome
Anaemia, thrombocytosis, clubbin
Common methods used to obtain material for histological diagnosis
Histological diagnosis necessary for cell type and prognosis
Bronchoscopy
Needle biopsy
Thoracocentesis
Diagnosis and staging of lung cancer
Initially CXR
Serum biochemistry
Imagining with ct, isotope bone scan, bronchoscopy
Tissue with biopsy
Give an account of he histology and classification of common lung tumours
Non small cell:
Squamous cell carcinoma (40%) - central angulate cells, eosinophilic, keratinisation (pearls)
Adenocarcinoma 35%- peripheral tumours, columnar/ cuboidal cells, acini, papillary structures, May line alveoli, may produce mucins
Large cell carcinoma
Small cell carcinoma 12%- less cytoplasm, small nuclei, nuclear moulding, necrosis and mitosis. Oat cell carcinoma
Behaviour of different cancer and prognosis and treatment
Most non small cell are inoperable but most small cell are metastatic so has a worse prognosis.
Different treatments for lung cancer
Surgery for NSS
Chemotherapy, potentially curative in NSS and can lead to improvements in SS
Radiotherapy- radical or palliative
Biological therapies- EGFR, immunotherapy
Combination therapy
Palliative care
Describe pleural effusion, pneumothorax, consolidation, space occupying lesion, lung collapse
Pneumothorax- black air trapped, visible pleural edge, tracheal shift away
Pleural effusion- loss of costs phrenic angles of hemidiaphragm, meniscus of fluid
Consolidation- dense opacification
SOL- nodule less than 3, mass larger. Causes malignancy, inflammation, congenital, benign mass legion
Lung collapse- elevation of hemidiaphragm, crowding of ribs, shift of mediastinum towards, crowding of pulmonary vessels, sail sign
Identify cardiac enlargement/ cardiac index
PA
Ratio of heart to rib age at largest. Normal is below 50%
Causes of ILS
Immunological - sarcoidosis- steroids, may be obstruction too
Connective tissue disorder- RA, SLE, scleroderma, polymyositis
Occupational- coal workers, farmers - extrinsic allergic alveolitis e.g. Bird fanciers lung, farmers, asbestososis
Idiopathic (50%)- IPF steroids, IIP no treatment
Treatment related- methotrexate, amioderone, nitroflurotoin, chemotherapy
Describe the involvement of different inflam cells in interstitial lung disease
Area inbetween air spaces for support, diffusion and repair
Epithelial, endothelial, macrophages, mesenchymal and other inflam cells
Clinical features of ILS.
SOB, reduced exercise tolerance, dry cough
Tachpnoea, tachycardia,reduced chest movements, coarse crackles, cyanosis, RHF, clubbing in CFA(crypto genic fibrosing alveolitis)
Restrictive
Effect on gas exchange
Reduced transfer factor
Fibrosis so dead space
Less compliance
Increased diffusion pathway
Lung function tests of ILS
Restrictive so decreased FVC
Lung diseases and occupations ILS
Diffuse fibrosis- asbestosis is
Modular fibrosis- pneumoconiosis, duct, silica, asbestos
Alveolitis- farmer, pigeon
Xray of ILS
Fibrosing alveolitis - small, micro modular shadowing, ragged heart boarder
Extrinsic allergic alv - acute micro nodules, chronic is almost normal then disease
Sarcoidosis- military modular shadowing, diffuse fibrosis
Asbestosis is- plaques, fibrosis, mesothelioma
Factors affecting formation and reabsorption of pleural fluid
Production of absorption failure
Production- increase in pressure, increase in interstitial fluid, increase in permeability e.g. Infection or malignancy, decrease in oncotic
Absorption- increase in BP, lymph blockage
Types of pleural effusion
Haemothorax
Chylothorax (lipid)
Empyema (pus)
Simple effusion (serous fluid)
Transudate / exudate
30g/litre
Transudate- difference in starling forces
Exudate- dilation or vasculature or leakage
Describe the characteristics and causes of pleurisy
Chest pain- if diaphragm then shoulder Pain on inspiration, cough, sneeze, laugh Small breaths Pleural rub can be heard Causes Autoimmune - RA, SLE Infection Cancer- mesothelioma (asbestos) Pneumothorax PE Unabsorbed effusion Can lead to pleural fibrosis
Describe chest wall abnormalities and motor/ neurological diseases that can affect breathing
Pertussis carcinatum and excavatum, kyphosis, scoliosis. Acquired deformities. Muscular dystrophy, Motor neurone disease, polio
Course of the oblique fisssures
T2 SP- anterior behind 6 costal cartilage
Course of the right horizontal fissure
4th rib from MAL to anterior edge
